Orthodontic tooth movement requires the precise application of force directed towards moving the tooth through the alveolar bone along the dental arch. Orthodontic tooth movement is thus an example of directed bone remodeling, i.e., the imposition of external forces to reshape bone is made possible by the "biological plasticity" of bone. The biological plasticity of bone is made possible by the coordinated activities of osteoblasts and osteoclasts in the alveolar bone that somehow respond to this external force. We propose that a calcium-conducting stretch channel in the surface membrane of osteoblasts is the mechanical transducer responsible for detecting force and converting its energy into a biological response. We shall show that very small changes in osmotic pressure (i.e., < 5%), which open stretch channels in other cells, cause a significant increase in cytoplasmic calcium (Ca) - a well-known second messenger that is responsible for activating osteoblasts. The effect of osmotic-evoked stretches of the surface membrane on Ca is reproducible and fully reversible. Moreover, this rise in Ca disappears when extracellular calcium is removed, suggesting that this osmotic-induced rise in Ca is due to an influx of Ca. Our goal is to characterize this channel in the osteoblast-like cells (NC3T-E1), as well as osteoblasts isolated from fetal rat calvaria, discover specific inhibitors, and investigate its hormonal sensitivity. Understanding how this channel works will not only establish how orthodontists are able to move teeth, but will also contribute to our understanding of osseo-integration of dental implants, maxillofacial development, and the effects of gravity on the skeleton.